Lesions of the cerebral cortex sustained early in life provoke system-wide repercussions that include substantial rewiring of remaining subcortical and cortical pathways. These repercussions contribute significantly to functional compensations by cortical neurons and to the sparing of cognitive and perceptual processes that are profoundly impaired following equivalent damage incurred by the mature brain. The long-term goal of the proposed work is to identify the classes of functions that are spared by the early cortical damage, and to identify the neural basis of the sparing. The specific aim of the proposed work is to investigate the contributions which the expanded visual pathway through LGN to cortical area PMLS makes to operations spared by early lesions of areas 17 and 18. Studies will be carried out on cats which incurred damage of areas 17 and 18 on the day of birth or at one month of age, and comparison data will be collected from intact cats and cats which incurred equivalent damage in adulthood. Two projects are proposed: 1) to reveal the components and obtain a measure of the strength-of-coupling in the expanded retino-LGN- PMLS pathway. From these data we will infer the types of visual signals that are transmitted through LGN to cortex; and, 2) to uncouple the expanded retino-LGN-PMLS pathway in mature cats to ascertain the contribution the pathway makes to the spared behaviors. A battery of behavioral tests will be employed for functions normally associated with area PMLS, with damaged areas 17 and 18, and with the X and Y signal streams. The behavioral tasks will reveal the importance of the retino- LGN-pathway expansions to the spared behaviors. The proposed work will provide detailed information on the capacities of the immature brain to compensate for perceptual and cognitive functions lost or impaired following equivalent damage of the mature cerebrum. The identification of these capacities is important for steering future anatomical, physiological and behavioral efforts directed at comprehending the consequences of early cerebral cortical damage, and for developing therapeutic strategies that attempt to enhance the sparing of cortical functions.